The purpose of this research is to explore the mechanism of luteolysis in the primate. This will be accomplished by relating the changes in luteinizing hormone (LH) and prostaglandin F2 alpha (PGF 2 alpha) receptor binding of the monkey corpus luteum (CL) throughout the luteal phase to changes in peripheral plasma concentrations of LH, estradiol, estrone, and progesterone as well as ovarian vein progesterone, estradiol, estrone, and the 13, 14-dihydro-15-keto-metabolite of PGF 2 alpha (PGFM) sampled at the same time. It is hypothesized that spontaneous luteolysis is an event initiated by increased estrogen production in the CL and mediated through intraovarian PGF 2 alpha synthesis; PGF 2 alpha causes the decrease in progesterone secretion by decreasing the gonadotropin binding to the CL (loss of receptor). Time course changes in LH and PGF receptors, ovarian secretory activity, and the in vitro biosynthetic responsiveness of the CL in vitro will be determined in unperturbed animals (descriptive studies), which will be a marker for the provocative studies. Estradiol and PGF2 alpha will be constantly infused (via the Alza osmotic pump) into the CL and changes in systemic and ovarian venous steroid, LH and PGFM observed. At defined days after the onset of administration, the CL will be excised and the LH and PGF2 alpha receptor binding assessed. CL tissue will also be incubated in vitro with human chorionic gonadotropin and cyclic-adenosine monophosphate to test its ability to synthesize progesterone; a small piece of tissue will be taken for histology so that structure to function comparisons can be made. Other agents, which may be implicated in the process of luteolysis, will be administered locally to the CL and peripheral concentrations of LH, estradiol, estrone, progesterone, and PGFM and menstrual cycle length recorded. These are: estrone (Alzet pump) tamoxifen (antiestrogen-Alza pump) and indomethacin (PG synthesis inhibitor-Alza pump).